CCRES AQUAPONICS

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  1. Atherosclerosis: A Silent Cardiovascular Condition that Kills 1 Person Every 3 Seconds High blood pressure, high levels of triglycerides, oxidation of Low Density Lipoprotein (LDL) cholesterol and lowering levels of High Density Lipoprotein (HDL) cholesterol are the primary cause that leads to oxidative stress and chronic inflammation in the vessels. This condition emerges at early age and gradually compromises vascular integrity leading to atherosclerosis at a later stage of a person lifespan. Atherosclerosis is a cardiovascular condition in which fat deposits and become oxidized along the inner lining of the artery walls. This silent yet deadly build up progressively thickens, hardens and eventually blocks the arteries leading to sudden and severe circulatory complications including vascular ischemia, stroke or heart attack. Cardiovascular and circulatory deaths related to atherosclerosis accounts for 29% of all deaths globally; the primary cause of death in EU (42%), Eastern Europe (48%), UK (39%), North America (49%), China (34%), South America (31%); Middle East (31%) and India (29%) – World Health Report, 2010. Salmon Consumption and Lower Incidence of Cardiovascular Diseases Among Japanese. Just a Coincidence? The cardiovascular and circulatory benefits of natural astaxanthin are evident among Japanese who are the uppermost consumers of food containing astaxanthin (AX) in the world and have the lowest incidences of heart diseases amongst developed countries. As the French paradox of cardiovascular health is connected to “sipping red-wine†and Italians longevity to “olive oil dressed†salads, Japanese cardiovascular resilience can be associated with consumption of “astaxanthin-soaked†salmon. In fact, a growing number of scientific evidence points to a robust link between natural astaxanthin and cardiovascular health – 30 cardiovascular specific research publications including 10 clinical studies. Research suggests that oral supplementation of astaxanthin may reduce the risks of cardiovascular diseases by reducing hypertension while enhancing blood rheology, capillary circulation and vascular resilience. The Effects of Astaxanthin on Atherosclerosis Prevention and Development Astaxanthin Increase HDL Cholesterol and Decrease Serum Triglycerides For every 1 mg/dl increase in good cholesterol HDL, the risk of cardiovascular diseases drops by 3%. In fact, baby boomers with low-HDL (> 40mg/dL) increase their chances of experiencing coronary events by 50%. Recent studies suggest that individuals with low HDL cholesterol who also have high triglycerides levels are 11 times more likely to develop cardiovascular diseases. Achieving a significant increase of HDL is notoriously hard because it requires drastic lifestyle changes, so often ending with modest results or sudden relapses. Recent research suggests that astaxanthin supplementation can support lifestyle changers by synergizing HDL increasing effect with decreased level of serum triglycerides. Two recent studies demonstrated that astaxanthin consumption can steadily increase HDL cholesterol in both healthy and less healthy individuals -both as preventive and therapeutic use. Yoshida et al., (2009) conducted the first ever randomized, placebo-controlled human study to evaluate astaxanthin effect on dyslipidemia and metabolic syndrome. Sixty-one hyper-triglyceride subjects between 42-47 years old (BMI 24 mg/kg), received 0 (placebo), 6 mg, 12mg, 18mg of astaxanthin daily for 12 weeks. While the placebo group did not change their existing condition, the astaxanthin groups increased their HDL cholesterol by 11%, 15% and 7% respectively and decreased their serum triglycerides level by 17%, 25% and 24% respectively (figure 1). Figure 1. Astaxanthin increase HDL cholesterol and decrease Serum Triglycerides (STR). Subjects with lower levels of HDL and higher levels of STR are 11 times more likely to develop cardiovascular diseases (Yoshida et al., 2009) 61 hyper- triglyceride subjects between 42-47 yo; (BMI 24 mg/kg), received 0 (placebo), 6 mg, 12mg, 18mg of astaxanthin per day for 12 weeks In a recent clinical study, 73 subjects between 20-60 years of age who received 4mg of natural astaxanthin per day for 4 weeks had their serum triglycerides level decreased by 25 %(Satoh et al., 2009). In another study conducted in Japan, 15 healthy adults increased their HDL by 6% after ingesting 9mg/daily of astaxanthin for 8 weeks (Matsumaya et al., 2010). In 2007, Hussein et al., has shown that astaxanthin reduced the size of fat cells in rats, which lead to a lower risk of cardiovascular complications and chronic inflammation (figure 2). Figure 2. Astaxanthin reduced the size of fat cells. Large cells usually indicate higher risk of fat-oxidation chronic inflammation and oxidative stress, which are the leading causes of cardiovascular diseases (x10) (Hussein et al., 2006) Astaxanthin Decrease Red Blood Cells Oxidation and Lipid-Peroxidation High levels of triglycerides and low levels of HDL also increase the likelihood of fat-oxidation in vessels and formation of "wounds" in the inner lining of artery walls (endothelium) leading to chronic inflammation and oxidative stress; this situation causes degradation, narrowing and thickening of arteries. Three recent clinical studies have robustly pointed to astaxanthin ability to reduce fat peroxidation in blood plasma. In a randomized-double-blind placebo study, 33 overweight subjects received 5mg or 20mg astaxanthin daily for 3 weeks. Their lipid peroxidation markers plasma MDA Level (mmol) and plasma ISP (ng/mL) decreased by 30% and 60% in average (Choi et al., 2011). In another randomized double blind placebo controlled study, 30 subjects between 50 and 69 years of age received 0 (placebo), 6 or 12mg astaxanthin daily for 12 weeks (Nakagawa et al., 2011). The amount of oxidized red blood cells (PLOOH um0l/ml) decreased by 17% and 24% respectively(figure 3). Figure 3. Astaxanthin reduces red blood cells oxidation (RBCO) in senior subjects. RBCO cells has high correlation with neuro-degenerative (eg. dementia) and cardiovascular diseases (eg. heart attack) (Nakagawa et al., 2011) 30 subjects (15 F and 15 M) between 50 and 69 years of age , BMI 27·5 kg/m2 received 0 (placebo), 6 or 12mg astaxanthin per day for 12 weeks In 2007, Karppi et al., conducted a randomized double blind conducted placebo controlled study with 40 non-smoking subjects between 19-33 years of age who received 0 (placebo) or 8mg of astaxanthin daily for 12 weeks. Their lipid peroxidation markers -plasma-15-hydroxy fatty acidsdecreased by 60% and plasma-12-hydroxy fatty acids by 36%. In 2000, Iwamoto et al., has also shown that astaxanthin inhibited LDL oxidation in human subjects. Professor Aoi from Kyoto Prefectural University, has shown that astaxanthin limits exercise-induced cardiac oxidation damage in mice. Astaxanthin Enhance Biomarkers of Anti-oxidant Healthiness in the Blood Plasma Low antioxidant activity in the blood correlates with high incidences of stroke, neurological impairment in stroke patients and cardiovascular diseases. Therefore, it is crucial to monitor the biomarkers of antioxidant capacity in the blood when assessing the efficacy of an active ingredient. In a randomized double blind study, 33 overweight subjects received 5mg or 20mg astaxanthin daily for 3 weeks. Their plasma Superoxide Dismutase Level (SOD) (U/mL) and Plasma Total Antioxidant Capacity (TAC) Level (mmol) increased 45% and 19% respectively. (Choi et al., 2011) (figure 4). Other studies have produced similar results using different assessment methods. In an open label clinical study, 35 postmenopausal women were treated with astaxanthin daily dose of 12 mg for 8 weeks (Yonei et al., 2009). Astaxanthin supplementation increased biological antioxidant potential in the blood plasma by 5% in 8 weeks. In addition, Camera et al., suggested that astaxanthin protects and synergize with our endogenous antioxidant systems (superoxide dismutase, catalase and glutathione) from early degradation when subjected to oxidative stress (Camera et al., 2008). Figure 4. Astaxanthin increases Plasma SOD Level and Plasma TAC level. Low levels of SOD and TAC correlates with higher incidences of stroke, neurological impairment and cardiovascular diseases (Choi et al., 2011) 33 subjects received 5mg or 20mg astaxanthin x day for 3 weeks; BMI (25.0 -30.0 kg/m2) - aged 25.Normal Body Subjects – 10 non-intervention subjects (20.0 < BMI≤24.9 kg/m2) age 26 Astaxanthin Decrease Chronic Inflammation that comprise Blood Vessels Integrity In the presence of oxidized cells in the endothelial lesions, macrophages white blood cells infiltrate in affected areas to clear away pathogens and dead cells. Yet, in the attempt to clean up the oxidized areas, macrophages may get overweighed with excessive lipoproteins and unable to leave the artery walls. This peculiar but common situation triggers a cascade of chronic inflammatory responses and pro-oxidant activities that degraded the structural integrity of the vessels. Therefore, up-regulated activity of oxidized LDL via macrophage induced inflammation is central to the initiation and progression of atherosclerosis. They are closely associated with plaque development, aggravation and ruptures. A recent study shows that astaxanthin decreased macrophage occupied lesion areas and therefore inflammation in the vessels of rabbits by 40% compared to control group (figure 5). Furthermore, rabbits that ingested 4mg astaxanthin everyday for 24 weeks decreased programmed cell death (apoptosis) by 42% and cell death (necrosis) by 17% in the aorta (Li et al., 2004). Figure 5. Astaxanthin decrease chronic inflammation and cell death in the inner lining of the vessels. Chronic inflammation and apoptosis in the endothelium dramatically accelerates vascular degradation and atherosclerotic plaque formation. (Li et al., 2004) Rabbits ingested 4mg of placebo, Vitamin E or astaxanthin everyday for 24 weeks. In-vitro study provides further evidences that astaxanthin (5-10uM) decreases macrophages related activation (SR-A and CD36) by 48% and 58% respectively (Kishimoto et al., 2009). A recent animal studies show that astaxanthin could ameliorate endothelial dysfunction by significantly improving the level of substances important for the regulation of vascular integrity. In more details, treatment with astaxanthin for 42 days decreased serum oxidized LDL cholesterol, aortic MDA levels, attenuated endothelium-dependent vasodilatory to acetylcholine, up-regulate eNOS expression and decreased LDL cholesterol receptor expression (figure 6). Figure 6. Astaxanthin treatment improved markers of endothelial dysfunction by reducing oxidation of LDL cholesterol and MDA. Higher levels of LDL oxidation and MDA expression highly correlates with structural damages in blood vessels and impairment of blood flow. (Zhao et al., 2011) Diabetic rats were treated with 10 mg/kg of astaxanthin or olive oil for 42 days. Animal studies have also shown that astaxanthin ameliorated structural changes in the blood vessels - reduction in wall thickness by 47% and improved vascular tone by 36% in spontaneously hypertensive rats (Hussein et al., 2006). Such structural changes was observed in the reduction of the number of branched elastin bands and improved vessel wall to lumen thickness ratio. In another study, 24 weeks supplementation of natural astaxanthin reduced levels of MMP3 expression in the aorta of rabbits - a crucial factor that lead to a degradation of elastin and collagen structures which determines the mechanical properties of connective tissues in the vessels (figure 7). In the experiment, astaxanthin enhanced plaque stability leading to a significant reduction of plaque ruptures (Li et al., 2004). Figure 7. Astaxanthin inhibit MMP over-expression in the thoracic aorta. Over-expression of MMP is a crucial factor that leads to the degradation of vascular integrity and escalation of atherosclerotic plaque ruptures (Li et al., 2004) Animal Study – Rabbits ingested AX 4mg/ Kg of body weight daily x 24weeks Astaxanthin Improving Vascular Resilience and Capillary Blood Flow Good circulation, quality of blood and resilient vessels are the key features required to fight development and progression of atherosclerosis. Blood rich in antioxidants bring nutrients and oxygen to organs while removing waste through a smooth vascular resilience and capillary flow. Recent human studies suggest that 6mg daily of astaxanthin can enhance blood flow by 10% in terms of capillary transit time -how fast the blood runs through the vessels (Miyawaki et al., 2008). Another complementary study showed that astaxanthin decreased lower limb vascular resistance by 17% - the degree to which the blood vessels impede the flow of blood (Iwabayashi et al., 2009).(figure 8) High resistance causes an increase in blood pressure, which increases the workload of the heart. In 2005, Nagaki et al., conducted another randomized double-blind study in which 36 subjects who received oral astaxanthin, 6mg/day for 4 weeks experienced a 4% improvement in capillary blood flow (Nagaki et al., 2005). Figure 8. astaxanthin decreased lower limb vascular resistance (LLVR) – the degree to which the vessels impede the flow of blood. LLVR increase blood pressure and circulatory complications that lead to peripheral vascular diseases, venous thrombosis and painful claudication (Yonei et al., 2009) 35 healthy postmenopausal women (BMI 22.1) were included in the study, treated with astaxanthin daily dose of 12 mg for 8 weeks. Astaxanthin Reduces Hypertension A series of human studies suggest that astaxanthin decreases blood pressure by improving blood flow and vascular tone. In a recent clinical study, 73 subjects, between 20-60 years of age, who received 4mg of astaxanthin for day for 4 weeks showed a significant decrease in systolic blood pressure (Satoh et al., 2009). In another study, 15 healthy subjects, between 27-50 of age, who received 9mg/day of astaxanthin for 12 weeks had their diastolic blood pressure decreased significantly (Matsuyama et al., 2010). A series of animal studies have largely replicated the effects of astaxanthin found in human studies (e.g. Ruiz et al., 2010; Preuss, 2011). Outlook Clinical studies suggests that oral supplementation of natural astaxanthin (4mg-12mg) may reduce the risk cardiovascular complications by enhancing blood rheology, lipid-metabolism, capillary circulation, vascular resilience and the endogenous antioxidant defense. Other clinical studies have also shown that astaxanthin reduce lipid-peroxidation, LDL cholesterol, blood pressure and DNA damage. Mechanism of action includes inhibition of macrophage-induced inflammation in the endothelium, oxidative stress-induced apoptosis and MPP-induced-structural degradation of the vessels. Furthermore, recent studies have also outlined that astaxanthin ameliorates nitric oxide dependent vessels dilation and reduce sensitivity to the angiotensin. References Aoi et al., (2003). Astaxanthin limits exercise-induced skeletal and cardiac muscle damage in mice. Antioxidants & Redox Signaling. 5(1):139-44. Hussein et al., (2005b). Antihypertensive potential and mechanism of action of astaxanthin II. Vascular reactivity and hemorheology in spontaneously hypertensive rats. Biol. Pharm. Bull., 28(6):967-971. Hussein et al., (2006b). Antihypertensive potential and mechanism of action of astaxanthin: III. Antioxidant and histopathological effects in spontaneously hypertensive rats. Biol. Pharm. Bull., 29(4):684-688. Hussein et al., (2005a). Antihypertensive and Neuroprotective Effects of Astaxanthin in Experimental Animals. Biol. Pharm. Bull., 28(1): 47-52. Iwabayashi et al., (2009). Efficacy and safety of eight-week treatment with astaxanthin in individuals screened for increased oxidative stress burden. Journal of Anti-Aging Medicine., 6(4):15-21 Iwamoto et al., (2000). Inhibition of low-density lipoprotein oxidation by astaxanthin. Journal of Atherosclerosis Thrombosis. 7(4):216-22. Karppi et al., (2007). Effects of astaxanthin supplementation on lipid eroxidation. Int J Vitam Nutr Jan; 77 (1): 3-11. Kishimoto et al., (2009). Astaxanthin suppresses scavenger receptor expression and matrix metalloproteinase activity in macrophages. European Journal of Nutrition., 49(2):17-26 Li et al., (2004). Alpha-tocopherol and astaxanthin decrease macrophage infiltration, apoptosis and vulnerability in atheroma of hyperlipidaemic rabbits. Journal of Molecular and Cellular Cardiology., 37:969-978. Matsuyama et al., (2010) A Safety Study on the Long-Term Consumption of Astaxanthin in Healthy Human Volunteer. Japanese Journal of Complementary and Alternative Medicine., (7):43-50. (Translated from Japanese) Miyawaki et al., (2005). Effects of Astaxanthin on Human Blood Rheology. Journal of Clinical Therapeutics and Medicines., 21(4):421-429.7. Murillo (1992). Hypercholesterolemic effect of canthaxanthin and astaxanthin in rats. Arch. Latinoam Nutr., 42(4):409-413. Preuss et al., (2009). Astaxanthin lowers blood pressure and lessens the activity of the eroxi-angiotensin system in Zucker Fatty Rats., Journal of Functional Foods., I:13-22 Yoshida et al., (2010). Administration of natural astaxanthin increases serum HDL-cholesterol and adiponectin in subjects with mild hyperlipidemia., 209 (2): 520-3. Nakagawa et al., (2011). Antioxidant effect of astaxanthin on phospholipid peroxidation in human erythrocytes British Journal of Nutrition., (31):1-9 Choi et al., (2011). Effects of Astaxanthin on Oxidative Stress in Overweight and Obese Adults Phytother. Research (in-press). Satoh et al., (2009).Preliminary Clinical Evaluation of Toxicity and Efficacy of a New Astaxanthin-rich Hameotoccus Pluvialis. J. Clin. Biochem. Nutr., 44: 280–284. Hussein et al., (2007). Astaxanthin ameliorates features of metabolic syndrome in SHR/NDmcr-cp. Life Sci., 16;80(6):522-9. Preuss, et al., (2011). High Dose Astaxanthin Lowers Blood Pressure and Increases Insulin Sensi-tivity in Rats: Are These Effects Interdependent?., 8(2):126-138. Ruiz et al., (2010). Astaxanthin-enriched-diet reduces blood pressure and improves cardiovascular parameters in spontaneously hypertensive rats. Pharmacological Research., 63(1):44-50 Zhao et al., (2011). Ameliorative effect of astaxanthin on endothelial dysfunction in streptozotocin-induced diabetes in male rats. Arzneimittelforschung., 61(4): 239-246. GD.......gratuitous acknowledgment removed.
  2. #Algae gets very little respect. Most people think of it as a nuisance: something green and slimy that glops up ponds. Actually we owe algae more than a little respect. We owe our existence to algae. The first species of algae evolved about 3.7 billion years ago. At that time the atmosphere was mostly CO2 and methane. Those are the two main greenhouse gases in the atmosphere. They are very good at reflecting heat back toward the earth and keeping it from escaping into space. Today they are present in our atmosphere in very tiny amounts. Imagine how hot it must have been with an atmosphere that was mainly CO2 and methane. Algae was the first organism that could use the energy from sunlight to turn carbon dioxide and water into sugar and oxygen. So, algae pretty much invented photosynthesis. By removing CO2 from the atmosphere and replacing it with O2, algae cleared the way for every organism on earth that breathes oxygen. Today, algae still rules the world when it comes to photosynthesis. It is responsible for about 70% of the oxygen produced on earth. "Think about that the next time you see a slimy pond", says Zeljko Serdar, President of #CCRES
  3. Where can money be invested today that will give the investor a reasonable rate of return and more importantly assure a safe investment that will be long lasting and be selling product into a growing and insatiable market? Go through the list of all of the possibilities you can think of, and then, add in these additional benefits to the equation: Produces food on a year round basis Can be solar powered Can use recycled water Employs local semi-skilled labor (women, men, young and old) Enhances the value of the property and surrounding property Is non-polluting Produces organic food and requires 90% to 95% less water than in-ground growing Can be installed nearly anywhere in the world Produces an organic fertilizer that can be used on any crop or plants All the food CCRES produced during the year is given to poor families. Take a look at our menu, and come visit us. Bon appétit! http://www.picocent.com/fun_page.php?fid=videos&v=EUfTaza7Vf4
  4. All the best from Croatia. CCRES TEAM http://ccresaquaponics.yolasite.com/
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  11. The Effects of Astaxanthin - Weight Control Physical Endurance and Muscle Recovery Work, Sport, Leisure – in fact all physical activity will generate reactive oxygen species (ROS); the more intense the activity the greater number of free radicals. ROS are shown to have damaging effects on muscle performance and recovery. Published and on-going research, focused on improving endurance and reducing recovery time, are showing dramatic benefits linked to the potent carotenoid - astaxanthin. These findings are bringing astaxanthin to the forefront as a dietary supplement for professional athletes and physically active people. Important to physical activity are our mitochondrial cells, often referred to as the “power stations of the cell†, which provide as much as 95% of our body’s pure energy (primarily by the burning of muscle glycogen and fatty acids). Unfortunately, a portion of this energy produces highly reactive and damaging ROS. ROS damage cells by triggering peroxidation of the cell membrane components, and oxidation of DNA and proteins. Furthermore, ROS continue to affect muscles even after the strenuous exercise has ceased. ROS activate the inflammation response whereby monocytes migrate into the muscle tissue causing additional cell damage. Often we will notice the onset of muscle damage during recovery in the form of tiredness and soreness. In addition to improving muscle performance through devised exercise regime, the sports research community is looking at other methods, such as nutrition to fuel and protect the body under extreme physical conditions. In the past, Vitamins E and C helped make the use of antioxidants a popular tool against oxidative damage during intense physical activity. Today, informed by current research we can point to astaxanthin as the antioxidant of choice for sports performance. Astaxanthin demonstrated 3 important physical benefits in clinical trials and supporting studies. Astaxanthin increased endurance, reduced muscle damage and improved lipid metabolism. Astaxanthin Boosts EnduranceIn a randomized, double-blind, placebo controlled study on healthy men supplemented with 4 mg astaxanthin per day for up to 6 months at Karolinska Institute, Sweden, standardized exercise tests demonstrated that the average number of knee bends performed increased only in the astaxanthin treated group at 3 months, and by the 6 month significant improvements were observed (Figure 1) (Malmsten & Lignell, 2008). Figure 1. Increase in strength/endurance (Malmsten & Lignell, 2008) Astaxanthin improved strength/endurance at 3 and 6 months determined by the average number of knee bends per person. Figure 2. Effect of astaxanthin on swimming time (Ikeuchi et al., 2006) Astaxanthin improves endurance in a dose-dependant manner. In another study, Aoi et al., (2008) demonstrated that astaxanthin may modify muscle metabolism by its antioxidant property and result in improved muscle performance and weight loss benefits. After 4 weeks the mice running time to exhaustion had significantly improved by up to 20 % , (2002) of Juntendo University, Japan, demonstrated by using 1200 meter track athletes, that a daily dose of 6 mg per day for 4 weeks resulted in their bodies accumulating lower levels of lactic acid (Figure 3). Ikeuchi et al., (2006) also reported the same findings and furthermore, astaxanthin efficacy had a dose-dependent response (Figure 4). Figure 3. Reduction of lactic acid build-up after astaxanthin supplementation in track subjects (Sawaki et al., 2002) Figure 4. Effect of astaxanthin on blood lactate during swimming for 15 minutes (Ikeuchi et al., 2006) Astaxanthin reduced build-up of lactic acid in a dose-dependant manner. In a double blind controlled placebo study, healthy women (n= 32; age-23-60) who ingested 12 mg of astaxanthin for 6 weeks significantly reduced their body fat (4%) when conducting routine walking exercise, compared to a placebo group. In addition, while control group increased their lactic acid by 31% compared to the astaxanthin group - only 13% The MechanismThe mechanism behind muscle endurance is based on several findings. Generally, astaxanthin protected the skeletal muscle from the increased damage of oxidative stress generated by physical activity. Furthermore, astaxanthin increased the metabolism of lipids as the main source of energy production by protecting the carnitine palmitoyltransferase I (CPT I) involved in fatty acid transport into mitochondria. Aoi et al., (2003) of Kyoto Prefecture University used mice models that may partially explain the efficacy of astaxanthin; they compared control, exercise placebo, and astaxanthin treated exercise groups after intense physical activity. 4-hydroxy-2-nonenal-modified-protein (4-HNE) stain analyses of the calf (gastrocnemius) muscles revealed significantly lower peroxidation damage (Figure 5). Figure 5. Effect of astaxanthin on 4-HNE-modifed proteins in leg muscle before and after exercise (Aoi et al., 2003) Other biochemical markers for oxidative damage and inflammation such as DNA, (2003) also explained that astaxanthin directly modulates inflammation caused by the release of the pro-inflammatory cytokines and mediators. In vivo and in vitro tests demonstrate that astaxanthin inhibits the IκB Kinase (IKK) dependant activation of the Nuclear Factor-kB (NF-κB) pathway, a key step in the production of pro-inflammatory cytokines and mediators. Aoi et al., 2008 also demonstrated increased lipid metabolism compared to carbohydrate as the main source of energy during strenuous activity (Figure 6). Furthermore, analysis of the mitochondrial lipid transport enzyme known as carnitine palmitoyltransferase I (CPT I) revealed increased fat localization (Figure 7) and reduction of oxidative damage in the presence of astaxanthin (Figure 8). CPT I is important because it regulates fatty acyl-CoA entry into the mitochondria in the oxidation of fatty acids in muscle. Exercise-induced ROS may partly limit utilization of fatty acid via diminishing CPT I activity. Figure 6. Fat substrate utilization increased with astaxanthin (Aoi et al., 2008) Calculated from the respiratory exchange ratio (RER) and oxygen consumption. Values are means ± SE obtained from 8 mice. Figure 7. Increased amount of FAT/CD36 that coimmunoprecipitated with CPT I skeletal muscle after a single session of exercise at 30 m/min for 30 min (Aoi et al., 2008) Values are means ± SE obtained from 6 mice. Figure 8. Astaxanthin reduced the amount of HEL-modified CPT1 in skeletal muscle after a single session of exercise at 30m/min for 30min (Aoi et al., 2008) Values are means ± SE obtained from 6 mice. Outlook Strenuous physical activity generates high levels of ROS which affect muscle performance and metabolism of lipids. New research shows that astaxanthin can modify muscle metabolism via its antioxidant effect, resulting in the improvement of muscle function during exercise. Therefore, astaxanthin is expected to be useful for physically active people as well as athletes. References Aoi W, Naito Y, Sakuma K, Kuchide M, Tokuda H, Maoka T, Toyokuni S, Oka S, Yasuhara M, Yoshikawa T. (2003). Astaxanthin limits exercise-induced skeletal and cardiac muscle damage in mice. Antioxid Redox Signal, 5(1):139-144. Aoi W, Naito Y, Takanami Y, Ishii T, Kawai Y, Akagiri S, Kato Y, Osawa T, Yoshikawa T. (2008). Astaxanthin improves muscle lipid metabolism in exercise via inhibitory effect of oxidative CPT I modification. Biochem. Biophys. Res. Com., 366:892–897. Fukamauchi, M. (2007). Food Functionality of astaxanthin-10: Synergistic effects of astaxanthin-10 intake and aerobic exercise. Food Style 21, 11(10). [in Japanese] Ikeuchi M, Koyama T, Takahashi J, Yazawa K. (2006). Effects of astaxanthin supplementation on exercise-induced fatigue in mice. Bio. Pharm. Bull., 29(10):2106-2110. Lee SJ, Bai SK, Lee KS, Namkoong S, Na HJ, Ha KS, Han JA, Yim SV, Chang K, Kwon YG, Lee SK, Kim YM. (2003). Astaxanthin Inhibits Nitric Oxide Production and Inflammatory Gene Expression by Suppressing IκB Kinase-dependent NF-κB Activation. Mol. Cells, 16(1):97-105. Malmsten C, Lignell A. (2008). Dietary supplementation with astaxanthin rich algal meal improves muscle endurance – a double blind study on male students. Carotenoid Science 13:20-22. Sawaki K, Yoshigi H, Aoki K, Koikawa N, Azumane A, Kaneko K, Yamaguchi M. (2002). Sports performance benefits from taking natural astaxanthin characterized by visual activity and muscle fatigue improvements in humans. J Clin.Therap. Med., 18(9):73- 88. CCRES special thanks to Mr. Mitsunori Nishida, President of Corporate Fuji Chemical Industry Co., Ltd. Croatian Center of Renewable Energy Sources (CCRES)
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  18. The Effects of Astaxanthin - Eye Health Astaxanthin for Eye Health The advances of information technology, software and electronics have led to the widespread use of screen based equipment or Visual Display Terminals (VDT) for both work and leisure. According to The National Center for Education Statistics, about 90 percent of children and adolescents in developed countries, ages 5 to 17, use computers at school or at home. About 50 percent of 9-year-olds use the Internet and at least 75 percent by ages 15 to 17. This phenomenon often lead to asthenopia or eye fatigue. The symptoms include sensitivity to glare, headaches, sore eyes and blurred vision. A recent study conducted by the National Institute of Occupational Safety and Health in USA found that over 90 percent of habitual users of VDT reported eyestrain and other visual problems associated with computer use. The American Optometric Association supported this in a survey reporting that between 50 and 75 percent of all VDT workers report eye problems. In another study conducted in Sweden, 23 percent of schoolchildren, aged 6-15 suffered from asthenopia-related symptoms (Anshel, 2009). Asthenopia prompted a large number of occupational safety studies. For example, epidemiological studies over the last decade revealed significant factors that contribute to eye fatigue. These studies, sometimes involving up to 6,000 sufferers identified the following causes: insufficient lighting, poor ergonomics and uncorrected vision. Despite the new information, follow-up studies later showed that the implemented improvements were only effective in 50% of sufferers. The possible explanations for this observation could be that other factors remained undiscovered, poor implementation of improvements, or visual work had become even more visually demanding. It is likely to be a combination of these factors so that current solutions are insufficient to reduce asthenopia. Standardized questionnaires that assessed subjective eye fatigue symptoms are in most cases mild, but symptoms get progressively worse if the causes are not rectified. Furthermore, certain ophthalmological tests can also detect eye problems, for example accommodation amplitudes, rate of accommodative reaction (positive and negative directions), critical flicker fusion (CFF) and pattern visual evoked potential (PVEP). So far, 10 Japanese clinical studies conducted by 9 independent ophthalmological establishments were able to conclude the efficacy of astaxanthin to alleviate visual asthenopia by observed improvements in the accommodation function and recovery of the ciliary body (Figure 1); retinal blood flow and inflammation markers. Figure 1. Location of the ciliary body in the human eye Astaxanthin Reduces Eye FatigueAsthenopia (eye fatigue) occurs on a daily cycle, in that the visual performance generally decreases naturally from morning until night. This problem exacerbates with a daily VDT load that lasts between 4 to 7 hours by affecting the accommodation performance of the ciliary body, which controls lens refraction. A couple of randomized double blind placebo controlled pilot studies demonstrated the positive effects of astaxanthin supplementation on visual function. For example, a study by Nagaki et al., (2002), demonstrated that subjects (n=13) who received 5 mg astaxanthin per day for one month showed a 54% reduction of eye fatigue complaints (Figure 2). In a sports vision study led by Sawaki et al., (2002), they demonstrated that depth perception and critical flicker fusion had improved by 46% and 5% respectively on a daily dose of 6 mg (n=9). The effect of astaxanthin on visual performance prompted a number of other clinical studies to evaluate the optimum dose and identify the mechanism of action. Figure 2. VDT Subjects with Eye Strain Symptoms before and after astaxanthin supplementation Overall, the 6 mg group improved significantly better at week 2 and 4 of the test period. Furthermore, questionnaire results obtained by Shiratori et al., (2005) and Nagaki et al., (2006), also confirmed the previous findings that astaxanthin supplementation at 6 mg for 4 weeks improved symptoms associated with tiredness, soreness, dryness and blurry vision. Another study by Takahashi & Kajita (2005), also demonstrated that astaxanthin attenuates induced-eye fatigue, as opposed to treating eye fatigue, which suggests prevention rather than treatment. Astaxanthin treated groups (asthenopia negative) were able to recover quicker than the control group after heavy visual stimulus. Later, Iwasaki & Tawara (2006) also confirmed the same tendencies of subjective eye fatigue complaints in a randomized double-blind placebo controlled double-crossover study.In addition to questionnaires, direct measurement associated with asthenopia is also strong indicators for understanding astaxanthin efficacy. These include accommodation amplitude (Figure 3); rate of accommodation reaction (positive and negative directions); CFF (critical flicker fusion) and PVEP (pattern visual evoked potential). Based on the quantitative information, the accommodation related measurements consistently improved after the treatment period (Nagaki et al., 2002, 2006; Nakamura et al., 2004; Takahashi & Kajita, 2005; Shiratori et al., 2005; Nitta et al., 2005; Iwasaki & Tawara, 2006) whereas the CFF and PVEP remained inconclusive (Sawaki et al., 2002; Nagaki et al., 2002; Nakamura et al., 2004). Therefore, the mechanism by which astaxanthin improved eye fatigue strongly indicates accommodation. Figure 3. Objective accommodation (Nitta et al., 2005) Objective accommodation amplitude improves with 6mg astaxanthin. Delaying Progression of PresbyopiaIn a questionnaire survey study conducted by Kajita et al. (2009), 77 percent of 22 elderly males (age 46-65), after ingested 6 mg of astaxanthin daily for 4 weeks, felt better about the subjective symptoms related to presbyopia – a reduced ability to focus on near objects caused by loss of elasticity of the crystalline lens after age 45. In more detail, participants felt an improvement when seeing nearby objects and a decrease in blurred vision. This was followed by alleviation of eye strain and shoulder stiffness. In addition, the pupillary constriction ratio, used to assess the accommodative function of the eye, showed an overall improvement of 19 percent after supplementation of astaxanthin. Therefore, Kajita et al. (2009) concluded that astaxanthin may slow down the progression of presbyopia in middle-aged and elderly people. Mechanism of Action Accommodation Improvement Accommodation measures the lens refractive property and it corresponds to the ciliary body function. This small ocular muscle controls the lens thickness in order to focus the light on the retina. In heavy visual workloads, the eye is focused on a fixed object distance for extended periods that will cause muscle spasms or develop fatigue detectable by accommodation tests. These tests are interrelated and include the following: accommodation amplitude; accommodation reaction (positive or negative) and high frequency component (HFC). Each clinical study used a combination of accommodation tests to indicate the amount of fatigue present. For example, increased accommodation amplitude in all treated subjects indicated improved reaction on near and far objects (Nagaki et al., 2002, 2006; Nakamura et al., 2004). Figure 4, Figure 5 and Table 1 reveal the higher rate of accommodation reactions measured in astaxanthin treated groups. These indicate the speed at which the ciliary body reacted to the direction change of focus (negative accommodation means from a near object at 35 centimeters to distant object at 5 meters or vice versa); (Nitta et al., 2005; Shiratori et al., 2005; Nakamura et al., 2005; Iwasaki & Tawara, 2006). The effects of astaxanthin are significant from 2 weeks. Table 1. Improvement of negative accommodation time with astaxanthin (Iwasaki & Tawara, 2006) Figure 4. Positive accommodation change (Shiratori et al., 2005) Rate of positive accommodation improves with 6 mg astaxanthin Figure 5. Negative accommodation (Shiratori et al., 2005) Rate of negative accommodation improves with 6 mg astaxanthin Another technique called HFC directly measured the microfluctuations in the lens during the accommodation response and typical values exist between 50 and 60 for normal eyes. Asthenopia sufferers (values greater than 60) experienced faster rates of recovery (Figure 6) in that their HFC results decrease towards normal values in less time compared to control groups (Takahashi & Kajita, 2005). Figure 6. Accommodative Recovery observing difference of HFC (Takahashi & Kajita, 2005) Astaxanthin improves HFC accommodation recovery during rest periods after visual work. Increased Blood-flow Figure 7. Increase of retinal blood flow (Nagaki et al., 2005) Retinal blood flow increases with astaxanthin after 4 weeks. Anti-inflammationLastly, a top Japanese ophthalmology research collaboration between Hokkaido, Yokohama and Tokyo concluded anti-inflammatory properties of astaxanthin in endotoxin-induced uveitis (EIU or eye inflammation) both in vivo and in vitro models.In another study, Suzuki et al., (2006) confirmed the same effects while they carefully studied the anti-inflammatory effect of astaxanthin in the iris-ciliary body of rat eyes. This was also the first study to prove that astaxanthin suppressed NF-kB activation by free radicals in the EIU rat model (Figure 8). The result is a lower pro-inflammatory response that would otherwise perpetuate local sites of inflammation that may also help explain why astaxanthin worked to alleviate eye fatigue in numerous clinical trials. Figure 8. Number of NF-κB positive cells in eye ciliary body during inflammation (Suzuki et al., 2006) Astaxanthin reduced the number of inflamed cells in the ciliary body. Outlook Eye fatigue or asthenopia is a common problem that occurs with the regular use of VDTs and may be resolved with findings from many worldwide epidemiological studies. However, if current improvements tend to be only 50% successful and other factors are likely to be involved, therefore, based on the current clinical evidence, astaxanthin offers a complementary alternative by reducing inflammation, improving accommodation and increasing blood flow. References Anshel D. J. (2009). Healthy Eyes Better Vision, Summerlin Publishing Group, USA. Fukuda M, Takahashi J, Nishida Y, Sasaki H. (2008). Intraocular penetration of astaxanthin in rabbit eyes. Atarashii Ganka, 25(10):1461-1464. [in Japanese] Hashimoto H, Arai K, Takahashi J, Chikuda M, Obara Y. (2009). Effect of Astaxanthin Consumption on Superoxidize Scavenging Activity in Aqueous Humor. Atarashii Ganka, 26(2): 229-234. [in Japanese] Iwabayashi M, Fujioka N, Nomoto K, Miyazaki R, Takahashi H, Hibino S, Takahashi Y, Nishikawa K, Nishida M, Yonei Y. (2009) Efficacy and safety of eight-week treatment with astaxanthin in individuals screened for increased oxidative stress burden. J. Anti Aging Med. 6 (4):15-21. Iwasaki T, Tawara A. (2006). Effects of Astaxanthin on Eyestrain Induced by Accommodative Dysfunction. Atarashii Ganka, (6):829-834. [in Japanese] Kajita M, Tsukahara H, Kato M. (2009). The Effects of a Dietary Supplement Containing Astaxanthin on the Accommodation Function of the Eye in Middle-aged and Older People. Medical Consultation & New Remedies, 46(3). [in Japanese] Miyawaki H, Takahashi J, Tsukahara H, Takehara I. (2005). Effects of astaxanthin on human blood rheology. J. Clin. Thera. Med., 21(4):421-429. Nagaki Y, Hayasaka S, Yamada T, Hayasaka Y, Sanada M, Uonomi T. (2002). Effects of astaxanthin on accommodation, critical flicker fusions, and pattern evoked potential in visual display terminal workers. J. Trad. Med., 19(5):170-173. Nagaki Y, Mihara M, Tsukuhara H, Ohno S. (2006). The supplementation effect of astaxanthin on accommodation and asthenopia. J. Clin. Therap. Med., 22(1):41-54. Nagaki Y, Miharu M, Jiro T, Akitoshi K, Yoshiharu H, Yuri S, Hiroki T. (2005). The effects of astaxanthin on retinal capillary blood flow in normal volunteers. J. Clin. Therap. Med., 21(5):537-542. Nakamura A, Isobe R, Otaka Y, Abematsu Y, Nakata D, Honma C, Sakurai S, Shimada Y, Horiguchi M. (2004). Changes in Visual Function Following Peroral Astaxanthin. Japan J. Clin. Opthal., 58(6):1051-1054. Nitta T, Ohgami K, Shiratori K, Shinmei Y, Chin S, Yoshida K, Tsukuhara H, Ohno S. (2005). Effects of astaxanthin on accommodation and asthenopia – Dose finding study in healthy volunteers. J. Clin. Therap. Med., 21(6):637-650. Ohgami K, Shiratori K, Kotake S, Nishida T, Mizuki N, Yazawa K, Ohno S. (2003). Effects of astaxanthin on lipopolysaccharide-induced inflammation in vitro and in vivo. Invest. Ophthal. Vis. Sci., 44(6):2694-2701. Sawaki K, Yoshigi H, Aoki K, Koikawa N, Azumane A, Kaneko K, Yamaguchi M. (2002) Sports performance benefits from taking natural astaxanthin characterized by visual activity and muscle fatigue improvements in humans. J. Clin. Ther. Med., 18(9):73-88. Shiratori K, Ohgami K, Nitta T, Shinmei Y, Chin S, Yoshida K, Tsukahara H, Takehara I, Ohno S. (2005). Effect of astaxanthin on accommodation and asthenopia – Efficacy identification study in healthy volunteers. J. Clin. Therap. Med., 21(5):543-556. Sussman M. (2001) Total Health At The Computer, Station Hill, New York. Suzuki Y, Ohgami K, Shiratori K, Jin XH, Ilieva I, Koyama Y, Yazawa K, Yoshida K, Kase S, Ohno S. (2006). Suppressive effects of astaxanthin against rat endotoxin-induced uveitis by inhibiting the NF-kB signaling pathway. Exp. Eye Res., 82:275-281. Takahashi N, Kajita M. (2005). Effects of astaxanthin on accommodative recovery. J. Clin. Therap. Med., 21(4):431-436. CCRES special thanks to Mr. Mitsunori Nishida, President of Corporate Fuji Chemical Industry Co., Ltd. Croatian Center of Renewable Energy Sources (CCRES)
  19. The Effects of Astaxanthin - Type 2 Diabetes Draining the World WealthDiabetes mellitus is a worldwide epidemic that is critically linked to prevalence of obesity. More than 220 million people have diabetes and by the year 2030 the figures are expected to grow to 360 million. The diabetes is aggressively growing in both emerging and developed country. According to WHO, the Asian continent has over 90 million people suffering from diabetes – India (40 million) China (29 million); Indonesia (13 million) and Japan (7 million). The prevalence of diabetic patients remains pervasive in USA (22 million), Brazil (6 million), Pakistan (8 million); Russia (6 million); Italy (5 million) and Turkey (4 million). Even in the African region over 10 million people suffer from diabetes, especially in Nigeria where it is expected to reach 5 million within the year 2030. Diabetic complications lead to heart disease (approximately 65% of death amongst diabetics), blindness, kidney failure and amputations. As a result, the indirect and direct medical expenditure of diabetics represent almost 5 times that of a non-diabetic. Type 2 Diabetes: A Preventable Disease In most cases, diabetes is treated with medication, although about 20% of diabetics may be managed by lifestyle changes. This means that even if we cannot change the genetic influences, fortunately, for most of us diabetes is preventable; for example, making dietary changes, taking nutritional supplements and exercising. To highlight this, people in high risk groups who achieve a 5-7% cut in body weight will reduce risk of developing diabetes approximately 58% across all age and ethnic groups. While the debate between the contributory effects of carbohydrate and fat intake continues unabated, research reveals a strong link between foods with high glycemic index and prevalence of type 2 diabetes. Excess blood glucose needs to be converted by insulin (produced by the pancreas ß-cells) into glycogen stores, however, when glycogen stores are full, glucose is converted into fat. Over time, the body’s cells may eventually become desensitized to insulin making it necessary to produce more insulin to achieve the same affect. It is this process that would eventually lead to a state known as hyperinsulinaemic state. As a result, the body looses its ability to control high blood glucose levels (hyperglycemia) that could result in toxic conditions and promote further complications such as kidney failure. New Evidences Emerging from Human StudiesIn an anti-aging study conducted by Iwabayashi et al., (2009), 20 female volunteers with increased oxidative stress burden ingested 12 mg/day of astaxanthin for 8 weeks. Results evidenced a significant decrease of diabetes-related parameters that collectively predict trends in diabetes development. Firstly, astaxanthin reduced cortisol by 23 percent. Astaxanthin Retards Glucose Toxicity and Kidney DamageAstaxanthin displayed positive effects in a type 2 diabetic mouse model in that it reduced the disease progression by retarding glucose toxicity and kidney damage. This has profound implications for people who belong to high risk groups, display pre-diabetic conditions (impaired fasting glucose or impaired glucose tolerance) or want to manage advanced diabetic kidney problems (nephropathy). Studies suggested that reactive oxygen species (ROS) induced by hyperglycemia contributes to the onset of Diabetes mellitus and its complications. Non-enzymatic glycosylation of proteins and mitochondria, prevalent in diabetic conditions, is a major source of ROS. For example, pancreatic ß-cells kept in high glucose concentrations show presence of advanced glycosylation products, a source of ROS, which cause the following: i) reduction of insulin expression and ii) induction of cell death (apoptosis). ß–cells are especially vulnerable to ROS because these cells are inherently low in antioxidant status and therefore, requires long term protection. A recent study demonstrated that antioxidants (N-acetyl-L-cysteine, vitamins C and E) exerted beneficial effects in diabetic conditions such as preservation of ß-cell function, so it is likely that a more potent antioxidant such as astaxanthin can do the same or better. In another study conducted by Preuss et al. (2009), 12 rats fed with 25mg/kg of astaxanthin show a significant decrease in insulin resistance by 13.5%. Modulation of Glucose ToxicityUchiyama et al., 2002 demonstrated in obese diabetes type 2 mouse model that astaxanthin preserved pancreatic ß -cell dysfunction against oxidative damage. Treated mice received 1 mg astaxanthin/day at 6 weeks of age and then tests performed at 6, 12 and 18 weeks. Observations of astaxanthin treated mice (N=8) included: i) significantly reduced fasting glucose sugar levels at 12. Figure 1. Astaxanthin improved the glucose levels in the Intraperitoneally Glucose Tolerance Test (IPGT) in diabetic mouse model (Uchiyama et al., 2002) Figure 2. Astaxanthin preserved insulin sensitivity in the diabetic mouse model (Uchiyama et al., 2002) Figure 3. Astaxanthin protected kidney function measured by urinary albumin protein loss (Naito et al., 2004) Prevention of Diabetic NephropathyAs well as substantiating observations by Uchiyama et al., Naito demonstrated that astaxanthin treated type 2 diabetic mice which normally shows renal insufficiency at 16 weeks of age in fact exhibited 67% less urinary albumin loss. Figure 4. Astaxanthin reduced the amount of DNA damage indicated by urinary 8-OHdG levels (Naito et al., 2004) Figure 5. Astaxanthin preserved the relative mesangial area. Earlier it was unclear how astaxanthin could ameliorate the progression of diabetic nephropathy, but new evidence revealed additional information in the mechanism of action. Naito et al., (2006) examined changes in the gene expression profile of glomerular cells in diabetic mouse model during the early phase of diabetic nephropathy. The mitochondrial oxidative phosphorylation pathway was most significantly affected by high-glucose concentration (mediated via reactive oxygen species). Long term treatment with astaxanthin significantly modulated genes associated with oxidative phosphorylation, oxidative stress and the TGF-ß-collagen synthesis system. Manabe et al., 2007 went further and analyzed normal human mesangial cells (NHMC) exposed to high glucose concentrations. In the presence of astaxanthin, it significantly suppressed ROS production (Figure 6) and inhibited nuclear translocation and activation of NF-ĸB (Figure 7) in the mitochondria of NHMC. Furthermore, this was the first time to detect astaxanthin in the mitochondrial membrane (Table 1) and its presence also suppressed ROS attack on membrane proteins. Figure 6. Astaxanthin reduced ROS production in NHMC-mitochondria exposed to high glucose (Manabe et al., 2007) Top left panel: mitochondria as green fluorescence, Top right panel: ROS as red fluorescence; Bottom right panel: Merged picture as yellow fluorescence. Figure 7. Astaxanthin suppressed high-glucose induced nuclear translocation and activation of NF-ĸB (Manabe et al., 2007) Table 1. Astaxanthin content in NHMC mitochondria expressed as percentage of total astaxanthin added. Mean of 3 samples. (Manabe et al., 2007) OutlookAlthough clinical trials involving antioxidants in humans have only recently begun, these preliminary results concluded that strong antioxidant supplementation may improve type 2 diabetic control and inhibit progressive renal damage by circumventing the effects of glycation-mediated ROS under hyperglycemic conditions. Astaxanthin improved pancreas function, insulin sensitivity, reduced kidney damage and glucose toxicity in diabetic mouse models. New techniques by gene chip analysis and fluorescence imaging revealed further details of mechanism and site of protection by astaxanthin. Further research and clinical studies are still required. However, it is reasonable to suggest that astaxanthin may be useful as part of a nutrigenomic strategy for type 2 diabetes and diabetic nephropathy. References Forefront (Summer/Fall) 2005, American Diabetes Association. Functional Foods & Nutraceuticals June 2004. "The dietary solution to diabetes." HSR Health Supplement Retailer July 2004. "Fighting Diabetes the natural way." Iwabayashi M, Fujioka N, Nomoto K, Miyazaki R, Takahashi H, Hibino S, Takahashi Y, Nishikawa K, Nishida M, Yonei Y. (2009). Efficacy and safety of eight-week treatment with astaxanthin in individuals screened for increased oxidative stress burden. J. Anti Aging Med., 6 (4):15-21. Manabe E, Handa O, Naito Y, Mizushima K, Akagiri S, Adachi S, Takagi T, Kokura S, Maoka T, Yoshikawa T. (2008). Astaxanthin protects mesangial cells from hyperglycemia-induced oxidative signaling. J. Cellular Biochem. 103 (6):1925-37. Naito Y, Uchiyama K, Aoi W, Hasegawa G, Nakamura N, Yoshida N, Maoka T, Takahashi J, Yoshikawa T. (2004) Prevention of diabetic nephropathy by treatment with astaxanthin in diabetic db/db mice. BioFactors 20:49-59. Nutritional Outlook April. "Fighting Diabetes" Naito Y, Uchiyama K, Mizushima K, Kuroda M, Akagiri S, Takagi T, Handa O, Kokura S, Yoshida N, Ichikawa H, Takahashi J, Yoshikawa T. (2006). Microarray profiling of gene expression patterns in glomerular cells of astaxanthin-treated diabetic mice: a nutrigenomic approach. Int. J. Mol. Med.,18:685-695. Preuss H, Echard B, Bagchi D, Perricone VN, Yamashita E. (2009). Astaxanthin lowers blood pressure and lessens the activity of the renin-angiotensin system in Zucker Fatty Rats. J. Funct. Foods, I:13-22. The Global Diabetes Community. http://www.diabetes.co.uk. Article retrieved on June 8th, 2010. Uchiyama K, Naito Y, Hasegawa G, Nakamura N, Takahashi J, Yoshikawa T. (2002). Astaxanthin Protects β–cells against glucose toxicity in diabetic db/db mice. Redox Rep., 7(5):290-293. CCRES special thanks to Mr. Mitsunori Nishida, President of Corporate Fuji Chemical Industry Co., Ltd. Croatian Center of Renewable Energy Sources (CCRES)
  20. Hi friends, Astaxanthin, a member of the carotenoid family, it is a dark red pigment and the main carotenoid found in algae and aquatic animals. It is responsible for the red/pink coloration of crustaceans, shellfish, and the flesh of salmonoids. CCRES produces astaxanthin from the microalga Haematococcus pluvialis, the richest known natural source for astaxanthin. Astaxanthin however, is more than just a red pigment, it is primarily an extremely powerful antioxidant. It has the unique capacity to quench free radicals and reactive species of oxygen and to inhibit lipid peroxidation. Studies have shown astaxanthin to be over 500 times stronger than vitamin E and much more potent than other carotenoids such as lutein, lycopene and β-carotene. Astaxanthin was found to have beneficial effects in many health conditions related to the Central Nervous System (CNS) disorders, skin health, joint health, muscle endurance, as well as to the cardiovascular, immune, eye and other systems. All the best from CCRES TEAM http://ccres-aquaponics.blogspot.com/2012/09/astaxanthin-from-haematococcus-pluvialis.html
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